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Phase 2a > resp conditions > Flashcards

resp conditions Flashcards

1
Q

define Chronic obstructive pulmonary disease (COPD)

what are the 2 main types

A

non-reversible, chronic deterioration in air flow thru. lungs caused by damage 2 tissue

x2 main types- chronic bronchitis, emphysema

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2
Q

list 4 risk factors for COPD

A
  • cigarettes/smoking
  • air pollution
  • genetic- A1AT
  • miners/coal workers
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3
Q

name 2 organisms that cause infective exacerbations of COPD

A
  1. H. influenza
  2. S. pneumonia

Abx= amoxicillin

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4
Q

describe chronic bronchitis + 3 presentations of it

A

daily cough w. sputum for 3+ months in @ least 2 consecutive years

  • hypertrophy + hyperplasia of mucous glands
  • chronic inflammation in bronchi + bronchioles = luminal narrowing
  • mucus hypersecretion, ciliary dysfunction, narrowed lumen
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5
Q

describe emphysema

A

destruction of elastin layer in alveolar ducts/sacs/resp bronchioles
- infammation + scarring= reduction in air flow + reduction in SA of aveoli

panacinar emphysema= A1AT def

centriacinar emphysema= smokers

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6
Q

typical presentation of Px with COPD

A

typically older patient w. chronic cough & purlulent sputum
+ extensive smoking history ( or A1AT)
+ SOB, cough, wheeze, recurrent resp infections
+ barrel chest/hyperinflation

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7
Q

describe ‘blue bloater’

chronic bronchtitis

A

cyanosis
chronic productive cough
purluent sputum
dyspnoea
peripheral oedema
obesity
recurrent chest infections

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8
Q

describe ‘pink puffer’

emphysema

A

minimal cough
pursed lip breathing
dyspnoea
accessory muscle breathing
cachexia (body/musc wasting)
barrel chest + hyperesonat precussion

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9
Q

investigations for COPD

A
  1. spirometry- FEV1/FEV <0.7= obstruction
  2. DLCO- diffuse capacity of CO across lung > COPD= low
  3. CXR- hyperinflation + exclude other causes eg cancer
  4. ABG- may show T2 resp failure
  5. genetic test for A1AT

**GOLD= clinical presentation + spirometry
bronchodilator irreversible (<12%) = COPD

bronchodilator reversible >12% = asthma

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10
Q

what can be used to guage the severity of COPD

A

MRC dyspnoea grading scale 1-5
1=breathless on strenuous excercise
5= cant leave home due 2 breathlessness

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11
Q

managment of COPD

1st,2nd,3rd

A

smoking cessaation + vaccines (pneumococcal vax + annual flu vax)

long term management=
1st. SABA (salbutamol) or SAMA (ipratropium bromide)

2nd. SABA + LABA (salmeterol) + LAMA (tiotropium bromide)

3rd. SABA + LABA + LAMA + ICS

consider long-term O2 therapy if severe sats <88%

maintain O2 88-92%

SABA= short-acting beta antagonist
SAMA= short-acting muscarinic antagonist
LABA= long-acting beta antagonist
LAMA= long-acting muscarinic antagonist

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12
Q

define asthma

A

chronic inflammatory condition caused by episodes of bronchoconstriction and mucus hypersecretion in response to triggers

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13
Q

list 6 things that can trigger asthma

A

cold air
excercise
allergens (cats, dust, pollen)
drugs (BB, ACEi,)
cigarette smoke
air pollution

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14
Q

what type of sensitivity is allergic asthma and what is mediated by

A

allergic (70% of asthma)
IgE mediated,, T1 hpersensitivity due 2 enviromental triggers

non- allergic = 30%- non IgE mediated (intrinsic)

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15
Q

what does IgE mast cell degranulation result in the releasing of

A

histamines
leukotrienes
tryptase
raised EOSINOPHILS

this causes bronchial constriction and mucus hypersecretion

ATPOPIC triad= (allergic rhinitis, atopic eczema and asthma)

chronic remodelling and mucus hypersecretion

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16
Q

presentations of asthma

A

episodes of:
* widespread polyphonic wheeze
* breathlessness
* chest tightness
* DRY cough
* usually worse @ night (diurnal variation)

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17
Q

investigations for asthma

A

PULMONARY FUNCTION TESTS!

Pathway as follows:

Fraction expired nitrous oxide (feNO) = raised (non specific in lung damage)

Then do Spirometry = FEV1:FVC less than 0.7 (obstruction)

Then do bronchodilator reversibility- >12% increase in FEV1 = reversible

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18
Q

how would you manage episodic/chronic asthma

episodic algorithm

A
  1. SABA (salbutamol)
  2. SABA + ICS (budesonide)
  3. SABA + ICS + LTRA (montelukast)
  4. SABA + ICS + LABA (salmeterol) +/- LTRA
  5. increase ICS dose
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19
Q

how would you manage acute exacerbations of asthma

A

OSHITME

Oxygen
SABA
HYDROCORTISONE (ICS)
IPRATROPIUM BROMIDE
THEOPHYLINE
MgSO4
Escalate care (BiPAP)

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20
Q

describe T1 resp failure

associated conditions? O2 and CO2? spirometry?

A

restrictive
-problem getting air in due 2 scarring

causes= (ILDs) pulmonary fibrosis, sarcoidosis, good pasture’s

low O2, normal CO2
FVC <0.8

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21
Q

describe T2 resp failure

associated conditions? O2 and CO2? spirometry?

A

problems getting air out
-more mucus + lumen blockage

causes= COPD, asthma, bronchiectasis

low O2, raised CO2

FEV1:FVC <0.7

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22
Q

what is mesothelioma

common exam presentation

A

lung cancer- plueral malignancy which affects pluera (and peritoneum)

male 40-70 w. ASBESTOS EXPOSURE DECADES AGO (long latent period)

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23
Q

presentation of mesothelioma

A

lung Sx= SOB, chest pain, constant cough + haemoptysis

recurrent laryngeal nerve compression= hoarse voice
bone pain

systemic Sxs=TATT, night sweats, wt.loss, rigors

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24
Q

investigations and managemnt for mesothelioma

A

1st= imaging (CXR then CT)= pluerall thickening +/- effusion

GOLD= biopsy

CA-125 may be raised non specifically

Tx= v. aggresive tumour- purely palliative

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25
Q

where does small cell lung cancer occur and who is affected

A

central resp system (bronchi)
-small cells w. minimal cytoplasm on biopsy

SMOKERS exclusively affected

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26
Q

presentation of small cell lung cancers

A

lung Sx= cough w. haemoptysis, SOB, recurrent chest pain

systemic (constitutional Sxs)
compression Sx

paraneoplastic syndromes

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27
Q

investigations and management of small cell lung cancers

A

1st= imaging (CXR then CT
GOLD= bronchoscopy then biopsy

v, early - can try chemo/radio - often just palliative

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28
Q

describe 5 neoplastic syndromes caused by small cell caricinomas

A
  1. SIADH= hyponatraemia
  2. raised ACTH= cushing’s
  3. carcinoid= flushing + diarrhoea
  4. lamberton eaton syndrome
  5. SVC syndrome (pemberton’s sign)
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29
Q

list 3 non-small cell lung cancers

A

squamous cell carcinoma
adenocarcinoma
carcinoid tumour

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30
Q

where do squamous cell carcinomas arise from, how does it present and who is most commonly affected

A

lung epithelium
mainly affects smokers

Lung Sx
constitutional Sx
compression Sx

PARANEOPLASTIC SYNDROME = PTHrP

metastises late

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31
Q

investigations and management of squamous cell carcinomas

A

1st= imaging (CXR then CT)
GOLD= bronchoscopy + biopsy
TNM staging

surgical excision, mets= chemo/radio

less aggresive than SCLC

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32
Q

where do adenocarcinomas arise from and what is a major risk facotr

A

arise from mucous secreting glandular epithelium
RF= ASBESTOS EXPOSURE

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33
Q

presentation of NSCLC adenocarcinomas + what are they closely related to

A

Lung Sx; Constitutional Sx, Compression Sx,

Metastasises common

Adenocarcinoma NSCLC is also closely related to HYPERTROPHIC
PULMONARY OSTEOARTHROPATHY

→ Triad of clubbing, arthritis and long bone swelling

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34
Q

investigations and managment for NSCLC adenocarcinomas

A

1st = Imaging (CXR then CT)
GS = Bronchoscopy + biopsy
TNM staging

surgical excision, if mets- radio/chemo
relatively treatable

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35
Q

what can compression of the sympathetic chain (T1-L2)in resp tumours cause

A

ipsilateral horner’s syndrome

  • miosis
  • ptosis
  • anhidrosis
  • right arm weakness
36
Q

what does pembertons sign look like and what does it indicate

A

raise arms above head + facial flushing = pemberton’s sign
-shows SVC obstruction due to compression

37
Q

what is mean pulmonary arterial pressure above in pulmonary HTN + give 4 causes

A

resting mPAP= >25mmHg
severe= 55+

causes=
* precapillary=primary pulmonary HTN, PE
* capillary= COPD, asthma
* post capillary= LV failure
* chronic hypoxemia= COPD, high altitude

38
Q

presentation of pulmonary HTN

what happens

A

reactive pulmonary vasoconstriction responding to hypoxemia= RVH + resp failure

  • exertional dyspnoea + fatigue 1st
    then
  • RV failure= raised JVP, periphera oedema
39
Q

investigations for pulmonary HTN

A

DIAGNOSTIC= RH catheter (directly measure pressure)

CXR= RVH
ECG= evidence of RA dilation (peaked p waves)

40
Q

management of pulmonary HTN + a comp

A

phosphodiesterase 5 inhibitor- sildenafil (viagra)

CCB- amilodipdine
prostaglandin analogues

comp= COR PULMONALE

41
Q

define goodpasture’s + common presentation

3 rfs

A

T2 hypersensitivity response resulting in pulmonary + renal pathology

EXAM= HAEMOPTYSIS + HAEMATURIA (aka coughing and pissing blood simultaneously)

HLA DR15, smoking, asbestos

42
Q

name antibodies in goodpasture’s + what they do

A

ANTI-GBM antibodies- attack basement membranes of alveoli + glomeruli- nephritic syndrome & alveolar haemorrhage

43
Q

presentation+ investigationm + managment for good pasture’s

A

lung= cough, haemoptysis, chest pain

renal= haematuria, HTN, oedema

Dx= serology: anti-GBM antibodies positive
lung + kidney biopsy= Ig complex formation

Tx= prednisolone + plasma exchange

44
Q

describe how TB is spread

A

TB spread via resp droplets (airborne infection)

  1. alveolar macrophages ingest bacteria- BUT resistant bacteria resist being killed > granuloma forms
  2. T cells cause necrosis to central part of granuloma= caseating granuloma (primary ghon focus)
  3. ghon focus spreads to nearby lymph nodes= ghon complex
  4. if TB spreads systemically= miliary TB
  5. most often contained within granuloma= latent TB
45
Q

describe the bacteria involved in Tuberculosis

A

mycobacterium infection
aerobic, non-motile, non-sporing slow growing bacilli w. thick waxy capsule

acid-fast bacilli- turns red/pink Ziehl- neelsen stain

resitant to phagolysosomal killing

Africa/S. asia

46
Q

systemic + pulmonary presentations of TB

A

systemic= wt. loss, low grade fever, night sweats, malaise

pulmonary= productive cough, haemoptysis, cough 3weeks +, SOB

47
Q

investigations for TB

+ Ix for latent TB

A

CXR
sputum culture for acid-fast bacili= Ziehl-Neelsen stain turns red/pink

biopsy= caseating granuloma

latent= tuberculin skin test ‘mantoux’
interferon gamma release assay

48
Q

describe the 3 kinds of pneumonia

A
  • community acquired= outside hospital enviroment
  • hospital acquired= after @ least 48hrs in hosptial + not intubated on admission
  • atypical= caused by atypical organisms not detectable by gram stain

pnuemonia= inflammation of air sacs in lungs caused by infection

49
Q

managment of TB

A

RIPE
Rifampicin x6months
Isoniazid x6months
Pyrazinamide x2 months
Ethambutol x2 months

SE=
rifampicin- haematuria
isoniazid- peripheral neuropathy
pyrazinamide- hepatitis, gout
ethambutol- optic neuritis

50
Q

list 4 organisms causing community accquired pnuemonia

A

streptococcus
s.pneumoniae
H.influenzae
haemophilius

51
Q

list 4 organisms causing hospital acquired pneumonia

A

psuedomonas aeruginosa
E.coli
S.aureus
klebsiella

52
Q

which organism causes pnuemonia in immunocompromised/HIV

A

(pneumocystis jirovecii) PCP

53
Q

name 2 organisms that cause atypical pneumonia

A

mycoplasma pneumoniae
legionella pneumophila

54
Q

a. which organism is likely to cause pneumonia associated with water cooler/air conditioner

A

legionella

55
Q

presentations of pneumonia

A

symptoms= cough, SOB, fever, pluertic chest pain

signs=
raised RR + HR
low BP + O2 sats
dull to precuss

auscultation= wheezing, coarse crackles, bronchial breath sounds, increased vocal resonance

56
Q

investigations for pneumonia

A

FBC= elevated WCC
sputum culture 2 ID organism
CXR= localised/widespread consolidation
effusion

57
Q

describe the scoring system used for pneumonia

A

CURB-65

Confusion
Urea >7mmol/L
resp >30
BP= <90 systolic, <60 diastolic

1 point for each

0-1= home treatment
2= short stay inpatient/closely monitored outpatient
3+ =hospital inpatient

58
Q

management of pneumonia

A

using CURB-65

0-1= oral amoxicillin
2= amoxicillin + clarithromycin
3+ = IV co-amoxiclav + clarithromycin

maintain O2 sats btwn 94-98%
analgesia= paracetamol/NSAIDs
IV fluids

59
Q

what is plueral effusion and describe the 2 causes

A

plueral effusion= collection of fluid btwn. parietal and visceral pluera of plueral cavity

transudative= fluid shift due to increase in hydrostatic/oncotic pressure (fluid overload, hypoalbuminemia, nephrotic syndrome) LOW PROTEIN COUNT

exudative= inflammation causes fluid + protein to leak into plueral space HIGH PROTEIN COUNT

60
Q

presentations of plueral effusion

A
  • SOB + cough
  • dull precussion over effusion
  • tracheal deviation away from effusion
61
Q

investigations for plueral effusion

A

1st= CXR> blunting of costophrenic angles

plueral USS

thoracocentesis ID + Dx underlying cause

62
Q

managent of plueral effusion

A

usually dependent on cause

  • heart failure- loop diuretics
  • infective- Abxs
  • malignant- therapeutic thoracentesis
  • large effusions= chest drain @ 5th intercostal space
63
Q

define a pneumothorax

list types

A

air in plueral space causing lungs to collapse
- plueral space= normally vaccum (negative intraplueral pressure)

spontaneous, tension

also: traumatic, latrogenic, lung pathology

64
Q

what is the typical patient with a pneumothorax

A

tall, thin male
with connective tissue disorder, smoker and has some kind of trauma

65
Q

presentation of a pneumothorax

A

symptoms= SOB, one sided sharp plueritic chest pain

signs= hyperresonant percussion note ipsilaterally + reduced breathing sounds

66
Q

investigations for a pneumothorax

A

1st + GOLD= CXR
* absent lung markings
* affected area darker than normal
* tracheal deviation to opposite side

67
Q

managment of a pneumothorax

A

Small PTX with no SOB = consider discharge and follow up CXR

Larger PTX and/or SOB = needle aspiration or chest drain (more of a longer term Tx)

Recurrent = surgical management - pleurodesis

68
Q

describe a tension pneumothorax

A

one way valve mechanism- air can flow into plueral space but can’t leave
-pressure increases w. each breath

69
Q

presentation and treatment of a tension pneumothorax

A
  • hypotension
  • resp distress
  • low sats
  • tachycardia
  • shock
  • severe chest pain

Tx= insert large bore cannula into plueral space @ 2nd intercostal space, midcalvicular line

70
Q

describe the mutation that occurs in cystic fibrosis

A

autorecessive mutation on chromosome 7- codes for CFTR protein

RFs= FHx + white

71
Q

describe the normal function of CFTR and what a defecit of it causes

A

CFTR normally secretes Cl- & Na + into ductal secretions > makes them thin and watery

defect= ductal secretions are thicker w. Na + & Cl - retention

> impared mucocillary clearance = stagnation of mucus= increased infection risk + difficulty breathing

72
Q

presentations of cystic fibrosis

resp, neonates, GI, other

A
  • Resp= recurrent infections, bronchiectasis
  • Neonates= jaundice, failure to thrive, bowel obstruction (meconium ileus)
  • GI= bowel obstruction, steatorrhea
  • other= male infertility, DM
73
Q

investigations for cystic fibrosis

A

newborn= heel prick test
older= sweat test > high chloride (+60)

reduced elastase
FHx + genetic testing

74
Q

management of cystic fibrosis

A

MDT approach:
chest physio & postural drainage, high calorie, high fat diet, minimise contact with ill people + others with CF, pancreatic supplmentation

comp= bronchiectasis

75
Q

define bronchiectasis

including causes

A

permanent dilation of the airways
-irreversible dilation, loss of cilia, mucus hypersecretion

causes= CF, lung cancer

76
Q

presentation and investigations for bronchiectasis

A

Sx= dyspnoea, cough, haemoptysis, recurrent chest infections

Dx=
CXR= kerley B lines, SIGNET RING SIGN (bronchioles dilated + appear thicker than adjacent pulmonary artery

sputum culture- H. influenzae mc.
GOLD= HRCT= dilated thickened bronchi

spirometry= FEV1: FVC <0.7

Tx= non-curative
chest physio + bronchodilators + prohylactic Abxs

77
Q

name 5 different types of interstitilal lung disease

A
  1. idiopathic pulmonary fibrosis
  2. sarcoidosis
  3. hypersensitivity pneumitis
  4. good pastures
  5. wegner’s granulomatis

ILD= umbrella term for lung pathology that causes lung fibrosis

78
Q

describe idiopathic pulmonary fibrosis

A

formation of scar tissue with no known cause
-seen in older men who smoke

Rfs= smoking, occupational (dust), drugs (methotrexate), EBV, CMV

progressive scarring = T1 resp failure

79
Q

presentation and investigations for idiopathic pulmonary fibrosis

A

dyspnoea, dry cough, bibasal crackles
Pulmonary Fibrosis:
3 C’s = Cynosis, Cough, Clubbing

Dx=
spirometry= restrictive lung disease FVC <0.8
GOLD=
HRCT > GROUND GLASS appearance of lungs

80
Q

management of interstitial lung disease

A

pirfenidone, nintedanib
non-pharm= smoking cessation, physio, vax

last resort= lung transplant

81
Q

describe sarcoidosis

who does it noramlly affect

A

idiopathic autoimmune granulomatous disease

20-40 y/o black women

82
Q

presentation of sarcoidosis

A

LUPUS PERNIO- purple rash/nodules on cheeks and shins
* fever
* fatigue
* dry cough
* dyspnoea
* uveitis

early= self resolving
sympto= corticosteroids

83
Q

describe hypersensitivity pneumonitis

type of hypersensitivity + rfs

A

T3 hypersensitivity (ab-ag complex deposition)= causes alveolar + bronchial inflammation after exposure to inhaled antigen

Rfs= farming keeping BIRDS

84
Q

presentation + investigations + management of hypersensitivity pneumonitits

A

dyspnoea, cough, fever, malaise, wt. loss

Dx= Hx + examination
serum IgG positive
-CXR= patchy nodular infiltrates
CT= ground glass shadowing

Tx= remove allergen + prednisolone

85
Q

what are the ABCDEF respiratory causes of clubbing

A

Respiratory Causes of
Clubbing: ABCDEF

Lung Abscess

Bronchiectasis

Cystic Fibrosis / Cancer

Decreased oxygen (hypoxia)

Empyema

Pulmonary Fibrosis

Phase 2a (12 decks)

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